Biological roles of crop NADP-malic enzymes and molecular mechanisms involved in abiotic stress

The abiotic stress tolerance of plants is very important for plant growth, development, survival and functional performance. NADP-ME is one of the most important enzymes in plants. Studying the role that NADP-malic enzyme plays in many metabolisms may help researchers improve the plant abiotic tolerance. The studies on NADP-ME in plants focus on its activity under different stresses. The regulation of NADP-ME gene expression in transgenic plants and the mechanism about abiotic stress resistance are less. In this paper, we reviewed the characteristics of the activity and genes expression of NADP-ME under drought, salt and temperature stresses. We also focused on the role of NADP-ME when it resists these varying stresses and the mechanism on how it performs.Key words: Plant NADP-malic enzyme, abiotic stress, gene expression, molecular mechanism

Ambient fabrication of flexible and large-area organic light-emitting devices using slot-die coating

The grand vision of manufacturing large-area emissive devices with low-cost roll-to-roll coating methods, akin to how newspapers are produced, appeared with the emergence of the organic light-emitting diode about 20 years ago. Today, small organic light-emitting diode displays are commercially available in smartphones, but the promise of a continuous ambient fabrication has unfortunately not materialized yet, as organic light-emitting diodes invariably depend on the use of one or more time- and energy-consuming process steps under vacuum. Here we report an all-solution-based fabrication of an alternative emissive device, a light-emitting electrochemical cell, using a slot-die roll-coating apparatus. The fabricated flexible sheets exhibit bidirectional and uniform light emission, and feature a fault-tolerant >1-μm-thick active material that is doped in situ during operation. It is notable that the initial preparation of inks, the subsequent coating of the constituent layers and the final device operation all could be executed under ambient air

Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function

<p>Abstract</p> <p>Background</p> <p>Previous studies demonstrated <it>Ganoderma lucidum </it>polysaccharides (GL-PS), a form of bioactive β-glucan can stimulate the maturation of monocyte-derived dendritic cells (DC). The question of how leukemic cells especially in monocytic lineage respond to GL-PS stimuli remains unclear.</p> <p>Results</p> <p>In this study, we used <it>in vitro</it> culture model with leukemic monocytic cell-lines THP-1 and U937 as monocytic effectors cells for proliferation responses and DCs induction. We treated the THP-1 and U937 cells with purified GL-PS (100 μg/mL) or GL-PS with GM-CSF/IL-4. GL-PS alone induced proliferative response on both THP-1 and U937 cells but only THP-1 transformed into typical DC morphology when stimulated with GL-PS plus GM-CSF/IL-4. The transformed THP-1 DCs had significant increase expression of HLA-DR, CD40, CD80 and CD86 though not as high as the extent of normal monocyte-derived DCs. They had similar antigen-uptake ability as the normal monocyte-derived DCs positive control. However, their potency in inducing allogeneic T cell proliferation was also less than that of normal monocyte-derived DCs.</p> <p>Conclusion</p> <p>Our findings suggested that GL-PS could induce selected monocytic leukemic cell differentiation into DCs with immuno-stimulatory function. The possible clinical impact of using this commonly used medicinal mushroom in patients with monocytic leukemia (AML-M4 and M5) deserved further investigation.</p

Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay

The decay channel $\psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p})$ is studied using a sample of $1.06\times 10^8$ $\psi^\prime$ events collected by the BESIII experiment at BEPCII. A strong enhancement at threshold is observed in the $p\bar{p}$ invariant mass spectrum. The enhancement can be fit with an $S$-wave Breit-Wigner resonance function with a resulting peak mass of $M=1861^{+6}_{-13} {\rm (stat)}^{+7}_{-26} {\rm (syst)} {\rm MeV/}c^2$ and a narrow width that is $\Gamma<38 {\rm MeV/}c^2$ at the 90% confidence level. These results are consistent with published BESII results. These mass and width values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics

Systemic properties of metabolic networks lead to an epistasis-based model for heterosis

The genetic and molecular approaches to heterosis usually do not rely on any model of the genotype–phenotype relationship. From the generalization of Kacser and Burns’ biochemical model for dominance and epistasis to networks with several variable enzymes, we hypothesized that metabolic heterosis could be observed because the response of the flux towards enzyme activities and/or concentrations follows a multi-dimensional hyperbolic-like relationship. To corroborate this, we used the values of systemic parameters accounting for the kinetic behaviour of four enzymes of the upstream part of glycolysis, and simulated genetic variability by varying in silico enzyme concentrations. Then we “crossed” virtual parents to get 1,000 hybrids, and showed that best-parent heterosis was frequently observed. The decomposition of the flux value into genetic effects, with the help of a novel multilocus epistasis index, revealed that antagonistic additive-by-additive epistasis effects play the major role in this framework of the genotype–phenotype relationship. This result is consistent with various observations in quantitative and evolutionary genetics, and provides a model unifying the genetic effects underlying heterosis

Epistasis: Obstacle or Advantage for Mapping Complex Traits?

Identification of genetic loci in complex traits has focused largely on one-dimensional genome scans to search for associations between single markers and the phenotype. There is mounting evidence that locus interactions, or epistasis, are a crucial component of the genetic architecture of biologically relevant traits. However, epistasis is often viewed as a nuisance factor that reduces power for locus detection. Counter to expectations, recent work shows that fitting full models, instead of testing marker main effect and interaction components separately, in exhaustive multi-locus genome scans can have higher power to detect loci when epistasis is present than single-locus scans, and improvement that comes despite a much larger multiple testing alpha-adjustment in such searches. We demonstrate, both theoretically and via simulation, that the expected power to detect loci when fitting full models is often larger when these loci act epistatically than when they act additively. Additionally, we show that the power for single locus detection may be improved in cases of epistasis compared to the additive model. Our exploration of a two step model selection procedure shows that identifying the true model is difficult. However, this difficulty is certainly not exacerbated by the presence of epistasis, on the contrary, in some cases the presence of epistasis can aid in model selection. The impact of allele frequencies on both power and model selection is dramatic

Histone deacetylase inhibitors: potential targets responsible for their anti-cancer effect

The histone deacetylase inhibitors (HDACi) have demonstrated anticancer efficacy across a range of malignancies, most impressively in the hematological cancers. It is uncertain whether this clinical efficacy is attributable predominantly to their ability to induce apoptosis and differentiation in the cancer cell, or to their ability to prime the cell to other pro-death stimuli such as those from the immune system. HDACi-induced apoptosis occurs through altered expression of genes encoding proteins in both intrinsic and extrinsic apoptotic pathways; through effects on the proteasome/aggresome systems; through the production of reactive oxygen species, possibly by directly inducing DNA damage; and through alterations in the tumor microenvironment. In addition HDACi increase the immunogenicity of tumor cells and modulate cytokine signaling and potentially T-cell polarization in ways that may contribute the anti-cancer effect in vivo. Here, we provide an overview of current thinking on the mechanisms of HDACi activity, with attention given to the hematological malignancies as well as scientific observations arising from the clinical trials. We also focus on the immune effects of these agents